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The Epstein-Barr virus (EBV) infects more than 90% of the human population,and is the cause of several both serious and mild diseases. It is atumorivirus, and has been widely studied as a model system for gene(de)regulation in human. A central feature of the EBV life cycle is its abilityto persist in human B cells in states denoted latency I, II and III. In latencyIII the host cell is driven to cell proliferation and hence expansion of theviral population, but does not enter the lytic pathway, and no new virions areproduced, while the latency I state is almost completely dormant. In this paperwe study a physico-chemical model of the switch between latency I and latencyIII in EBV. We show that the unusually large number of binding sites of twocompeting transcription factors, one viral and one from the host, serves tomake the switch sharper (higher Hill coefficient), either by cooperativebinding between molecules of the same species when they bind, or by competitionbetween the two species if there is sufficient steric hindrance.

Cooperative action in eukaryotic gene regulation: physical properties of a viral example